Despite an upregulation of TGFB1 in fibroblast clusters in MFS, our data support an overall decrease in canonical and non-canonical TGF-β signaling in advanced aneurysmal disease in MFS and suggest this decrease, particularly in SMCs, may be responsible for an overall less-differentiated contractile SMC phenotype. This evidence concerns the gene TGFB1 and Vascular dilatation.